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At least 631 records · Page 35Linked to original sources
PubMed1986

The autofluorescent "lipofuscin granules" in the intestinal cells of Caenorhabditis elegans are secondary lysosomes.

The nematode Caenorhabditis elegans contains autofluorescent lipofuscin granules, located exclusively in the 32-34 intestinal cells. Using epifluorescence microscopy on live adult animals, we have shown that fluorescent-labeled exogenous probes are taken up by endocytosis and accumulate within the granules. Macromolecular solutes such as proteins and dextran appear to be taken up by fluid-phase pinocytosis. There is no phagocytosis of latex particles with diameter greater than or equal to 0.25 micron. The granules concentrate the lysosomotropic weak base acridine orange, indicating that they have an acidic internal milieu. These observations imply that the lipofuscin granules in the intestinal cells are secondary lysosomes which remain active recipients of endocytosed materials.

Acridine Orange↗
PubMed1992

Redundancy in the microfilament system: abnormal development of Dictyostelium cells lacking two F-actin cross-linking proteins.

We generated by gene disruption Dictyostelium cells that lacked both the F-actin cross-linking proteins, alpha-actinin and gelation factor. Several major cell functions, such as growth, chemotaxis, phagocytosis, and pinocytosis, were apparently unaltered. However, in all double mutants, development was greatly impaired. After formation of aggregates, cells were very rarely able to form fruiting bodies. This ability was rescued when mutant and wild-type strains were mixed in a ratio of 70 to 30. The developmental program in the mutant was not arrested, since the expression pattern of early and late genes remained unchanged. Development of the mutant was rendered normal when a functional alpha-actinin gene was introduced and expressed, showing the morphogenetic defect to be due to the absence of the two F-actin cross-linking proteins. These findings suggest the existence of a functional network allowing mutual complementation of certain actin-binding proteins.

Actin Cytoskeleton↗
PubMedDate not supplied

Resistance of macrophages to 5-fluorouracil treatment.

The effect of 5-fluorouracil (5-FU) on murine monocytes and macrophages was the subject of this study. This drug strongly decreased the levels of all types of peripheral blood cell, but had no effect on the composition and cellularity of peritoneal exudate or the expression of Ia antigens or phagocytic activity of peritoneal macrophages. The pinocytic activity of normal macrophages was unchanged, but the pinocytosis of thioglycollate-stimulated macrophages was significantly reduced. The expression of Fc receptors was influenced only after the first day after 5-FU injection. The clearance and organ distribution of radioactive labeled antigen was also not changed. Our findings suggest that tissue macrophages are resistant to 5-FU, but the results obtained with stimulated macrophages suppose differential susceptibility of macrophages. We presume that the immunosuppressive action of 5-FU results from selective depletion and suppression of T and B lymphocytes rather than from changes in immunoregulating functions of macrophages.

Animals↗
PubMed1992

Sulfate metabolism in Entamoeba histolytica.

Sulfate fluxes and sulfate metabolites in Entamoeba histolytica were characterized employing [35S]sulfate as a marker. Sulfate was taken up both across the plasma membrane and by pinocytosis; in growth medium (sulfate concentration, 1.1 mM) total uptake was 1.5 mumol h-1 (5 x 10(7) cells)-1. The fate of sulfate within the cells was investigated by thin-layer chromatography. Major metabolites (together greater than 3 mumol (5 x 10(7) cells)-1) were monoethyl sulfate and 3-cholesteryl sulfate; both these products were released into the growth medium. As minor components we identified the activated sulfate derivatives, adenosine-5'-phosphosulfate and 3'-phosphoadenosine-5'-phosphosulfate. In addition, up to 10% of the sulfate taken up was incorporated into high-molecular weight material (possibly proteoglycans). We propose that sulfurylation of cholesterol may play a role in controlling membrane sterol content.

Adenosine Phosphosulfate↗
PubMed1982

The characterization of the uptake of avidin-biotin complex by HeLa cells.

HeLa cells have been shown to internalize the avidin-biotin complex. Adsorptive pinocytosis seems to be the mechanism of this uptake as seen by the requirements of energy and the integrity of the microtubular assembly. Pretreatment of HeLa cells with cycloheximide inhibits uptake and binding of the avidin-biotin complex. Scatchard plot of specific binding of avidin indicates a single type of binding with a Kd of approx. 55 pM with about 21,500 receptors/cell. The lack of inhibition of binding by simple carbohydrates indicates that binding is not through the oligosaccharide chain of avidin.

Avidin↗
PubMed1993

Platelet alpha-granules.

Platelets contain a vast number of biologically active molecules within cytoplasmic granules which are classified according to their respective distinct ultrastructures, densities and content. The alpha-granule is a unique secretory organelle in that it exhibits further compartmentalization and acquires its protein content via two distinct mechanisms: (1) biosynthesis predominantly at the megakaryocyte (MK) level (with some vestigial platelet synthesis) (e.g. platelet factor 4) and (2) endocytosis and pinocytosis at both the MK and circulating platelet levels (e.g. fibrinogen (Fg) and IgG). The currently known list of alpha-granular proteins continues to enlarge and includes many adhesive proteins (e.g. Fg, von Willebrand factor (vWf) and thrombospodin (TSP)), plasma proteins (e.g. IgG and albumin), cellular mitogens (e.g. platelet derived growth factor and TGF beta), coagulation factors (e.g. factor V) and protease inhibitors (e.g. alpha 2-macroglobulin and alpha 2-antiplasmin). More recently the inner lining of the alpha-granule unit membrane has been demonstrated to contain a number of physiologically important receptors including glycoprotein IIb/IIIa (alpha IIb beta 3) and P-selectin. The alpha-granules originate from small precursor granules which can be observed budding from the trans-Golgi network within the platelet precursor cell the MK. During MK maturation the alpha-granules become very prominent and are ultimately packaged into platelets during thrombopoiesis. The alpha-granular contents are destined for release during platelet activation at sites of vessel wall injury and thus play an important role in haemostasis, inflammation, ultimate wound repair and in the pathogenesis of atherosclerosis.

Animals↗
PubMedDate not supplied

Kinetics of endosomal acidification in Dictyostelium discoideum amoebae. 31P-NMR evidence for a very acidic early endosomal compartment.

We have examined the pH of the various endosomal compartments in the amoebae of the cellular slime mould Dictyostelium discoideum. This was accomplished both by fluorescence and by in vivo 31P-NMR methods. The fluid-phase marker, fluorescein-labeled dextran, was fed to the amoebae to report the average pH of their endocytic vesicles. During the progressive loading of successive endosomal compartments, we observed an early acidification down to a minimum value of pH < or = 5.3 after 30 min at 20 degrees C followed by an increase to an average pH of 5.8 when all the endosomal compartments were loaded by the fluid-phase marker. The weak fluorescence intensity of FITC-dextran at acidic pH precluded a more detailed investigation and we checked various phosphonate compounds as potential 31P-NMR pH probes for the endosomal compartments. Two molecules, aminomethylphosphonate and 2-aminoethylphosphonate, were selected for this study because of the large amplitudes of their chemical shift variation with pH (2 and 2.5 ppm, respectively) and their acidic pKs of 5.5 and 6.3, respectively. They were only moderately toxic (IC50% approximately 10 mM) towards both the axenic growth and the differentiation program of Dictyostelium amoebae. Internalization of the two aminophosphonates occurred only through the fluid-phase pinocytosis pathway as revealed by the full inhibition of their entry with 1 mM vanadate or 7.5 mM caffeine, two previously characterized inhibitors of endocytosis in Dictyostelium. We found that in vivo 31P-NMR of amoebae suspensions incubated with the aminophosphonates allowed the detection of three distinct intracellular compartments at pH 4.3, 5.8-6.0 and 7.3. Kinetics of aminophosphonate entry were analyzed and the results allowed us to reconstruct the time course for the acidification sequence during endocytosis. The data are consistent with the hypothesis that in Dictyostelium amoebae phosphonates occupy a highly acidic early endosomal compartment (t1/2 = 18 min; pH 4.3) before reaching a less acidic late endosomal/prelysosomal compartment (pH 5.8-6.0) from where they are immediately transported to, and trapped in, the cytoplasm (pH 7.3).

Acids↗
PubMed1986

Distant blood-brain barrier opening in subfields of the rat hippocampus after intrastriatal injections of kainic acid but not ibotenic acid.

Blood-brain barrier (BBB) permeability towards proteins was determined in rats 4 h after intrastriatal kainic or ibotenic acid application, using Evans blue as indicator. Whereas, with the exception of the unspecific damage in cortex, after ibotenic acid BBB remained intact in deep brain areas. Evans blue leakage was found ipsilateral to the kainic acid injection, occasionally in striatum, thalamus and amygdala and regularly in hippocampus. There it was confined to the fimbria and the CA3 field. Only rarely a mirror focus-like staining was present in the contralateral hippocampus. The ultrastructural investigation revealed that BBB opening in CA3 is due to increased transendothelial pinocytosis; the tight junctions were intact. Thus, changes in the microenvironment around vessels, elicited by kainic acid and/or seizures, might be responsible for BBB opening.

Animals↗
PubMed1978

Cell disease: desialylation of beta-hexosaminidase and its effect on uptake by fibroblasts.

The pinocytosis by fibroblasts of beta-hexosaminidase (EC 3.2.1.30) excreted by cultured skin fibroblasts from a patient with I-cell disease was not enhanced by neuraminidase treatment of the enzyme. The uptake of sialic acid-rich normal plasma beta-hexosaminidase was minimal and neuraminidase treatment did not appreciably enhance uptake. In contrast, sialic acid-rich normal seminal fluid beta-hexosaminidase was readily pinocytosed regardless of neuraminidase treatment. Thus the presence of sialic acid on beta-hexosaminidase does not influence uptake and a neuraminidase deficiency in I-cell disease may not be directly responsible for excessive extracellular enzyme.

Cells, Cultured↗
PubMed1985

Characterization of the adsorptive pinocytic capture of a polyaspartamide modified by the incorporation of tyramine residues.

Previously it has been shown (Duncan, R., Starling, D., Rypácek, F., Drobník, J. and Lloyd, J.B. (1982) Biochim. Biophys. Acta 717, 248-254) that incorporation of tyramine residues into poly (alpha, beta-(N-2-hydroxyethyl]-DL-aspartamide (PHEA) greatly increases its rate of pinocytic uptake by rat visceral yolk sacs cultured in vitro. Here we describe the relationship between the tyramine content (1.2-21.9 mol%) of modified PHEA and its rate of uptake by yolk sacs. Above a level of substitution of approximately 10 mol% the rate of uptake rises rapidly, and the concentration-dependence of capture is indicative of uptake by adsorptive pinocytosis. Serum proteins were shown to compete effectively for membrane binding sites, indicating a nonspecific interaction of PHEA-derivatives with the yolk sac membrane. PHEA derivatives of the same tyramine content, but of different mean molecular weights (Mr), were captured at the same rates.

Adsorption↗
PubMed1984

The blood-brain barrier in hypoxia: ultrastructural aspects and adenylate cyclase activity of brain capillaries.

The ultrastructure of brain microvessels, their permeability to serum albumin, the activities of some endothelial enzymes and the effect of histamine were investigated in rats after a prolonged hypobaric-hypoxic treatment. After prolonged hypoxia, the permeation of serum albumin into endothelial cells increased together with the number of pinocytotic vesicles of the endothelium. Intracarotid histamine stimulated this process even further, and its effect was mediated by H2-histamine receptors. After hypoxia the specific activity of capillary alkaline phosphatase and gamma-glutamyl transpeptidase remained unchanged, while that of adenylate cyclase was greatly increased. Histamine did not modify the structure of tight junctions of isolated capillaries of normoxic animals. Both hypoxia- and histamine-induced modification of the brain microvessels were accompanied by an increase of pinocytosis, which may be stimulated by the activation of capillary adenylate cyclase.

Animals↗
PubMed1985

Permeability of the blood-brain barrier to neuropeptides: the case for penetration.

Evidence that peptides can cross the blood-brain barrier (BBB) is reviewed. Penetration is suggested by the observations that blood levels correlate with cerebrospinal fluid levels for many peptides and that peripheral administration of peptides results in effects on the CNS. Passage is confirmed by experiments involving administration of a peptide (immunoactive or radioactive) in one compartment and identification of its appearance in the other, supported by such methods as selective labeling, cross-reactivity with highly specific antibodies, and chromatography. The degree of passage varies among peptides and their analogs. The major route of passage is probably by a non-competitive, non-saturable mechanism, wih the physicochemical characteristics of the peptide (e.g. lipophilicity, charge, molecular weight, and protein binding) determining the degree of passage. A competitive transport mechanism also exists for some peptides. Penetration of the BBB via large pores or by pinocytosis does not appear to be of major importance for peptides. Permeability of the BBB to peptides, but not to the larger iodinated albumin, is affected by intraperitoneal administration of aluminum, apparently by an increase in the permeability of the membrane to lipophilic materials.

Aluminum↗
PubMed1978

Uptake of protein by cultured human trophoblast cells.

The uptake of peroxidase by cultured human trophoblast cells was monitored ultrastructurally. There was no apparent effect on the distribution of peroxidase caused by treatment at 4 degrees C, with KCN or with IgG. Pinocytic channels penetrate deep into the perinuclear cytoplasm and may act to allow pinocytosis to occur within layers of microfilaments which might otherwise prevent pinosome access to the majority of the synthetic organelles.

Cell Membrane↗
PubMed1989

Anti-kidney antibody teratogenesis: evidence for a direct action on the rat conceptus by a mechanism involving the yolk sac.

IgG from anti-rat kidney antiserum (anti-K) was added to 48-h cultures of 9.5-day whole rat conceptuses. At concentrations of 25 micrograms/ml and above, dysmorphogenesis of embryos (optic vesicle defects) was observed. Significant embryonic growth retardation was apparent at 75 micrograms/ml and above. Other abnormalities (neural tube defects, deficits in axial rotation, reduced somite numbers) were seen at 100 and 150 micrograms/ml. In separate experiments, anti-K inhibited pinocytosis of 125I-polyvinylpyrrolidone by isolated yolk sacs. All of these effects of anti-K are similar to those produced by anti-visceral yolk sac antiserum suggesting a similar mechanism of teratogenic action, namely interference with yolk-sac-mediated embryotrophic nutrition.

Abnormalities, Multiple↗
PubMedDate not supplied

Inhibition of yolk sac function in late gastrulation rat conceptuses as a cause of teratogenesis: an in vivo/in vitro study.

A rabbit anti-rat yolk sac antiserum, administered by intraperitoneal injection at 0.25 mL/100 g bodyweight into 8.5-day pregnant rats, resulted in a resorption incidence of 20%, and growth retardation and malformation of all surviving fetuses at term. In all subsequent experiments, pregnant rats either received this same dose of antiserum at 8.5 days or were untreated. When 9.5-day rat conceptuses were cultured for 48 h in a medium containing serum from a 9.5-day pregnant rat that had been treated with antiserum, development was severely abnormal, regardless of whether conceptuses were explanted from antiserum-treated or untreated dams. In contrast, culture for 48 h in serum from untreated 9.5-day pregnant rats resulted in normal growth and development of conceptuses explanted from untreated dams, and in slight growth retardation and dysmorphogenesis in 9.5-day conceptuses explanted from antiserum-treated dams. In the former, development was similar to that attained by 11.5-day conceptuses from untreated dams; in the latter, development was appreciably better than in 11.5-day conceptuses from antiserum-treated dams. These results indicate that the critical period of exposure of embryos in utero to teratogenic antiserum after administration to the 8.5-day pregnant rat is longer than 24 h and that a significant insult is delivered to the conceptus before 9.5 days ea. Using 9.4-day ea conceptuses in culture, pinocytosis (uptake of 125I-labelled polyvinylpyrrolidone) by the yolk sac, and its inhibition by antiserum, was demonstrated. No pinocytic activity was evident in the embryo itself. These data support the hypothesis that anti-yolk sac antiserum exerts its teratogenic action by inhibiting the nutritional function of the yolk sac during early organogenesis.

Animals↗
PubMed1994

Changes in brain microvessel endothelial cell monolayer permeability induced by adrenergic drugs.

Brain microvessel endothelial cell monolayers have been shown to be a suitable blood-brain barrier in vitro system to study adrenergic regulation of permeability. We tested adrenergic drugs on bovine brain microvessel endothelial cell monolayer permeability to a biomembrane impermeant molecule, sodium fluorescein. Endogenous catecholamines noradrenaline and adrenaline were tested as well as the alpha-adrenoceptor agonist phenylephrine, the beta-adrenoceptor agonist clenbuterol and the alpha-adrenoceptor antagonist prazosin. Results showed an alpha-adrenoceptor mediated increase and a beta-adrenoceptor mediated decrease in monolayer permeability. Both alpha- and beta-adrenoceptor mediated changes in permeability were abolished by inhibiting fluid-phase pinocytosis, either by vincristine or by avoiding bovine brain microvessel endothelial cell's energy utilization. The reverse transport (i.e., from brain to blood side) was also influenced by adrenergic drugs; alpha- or beta-adrenoceptor stimulation induced a permeability-reducing effect. We conclude that alpha-adrenoceptor stimulation increases bovine brain microvessel endothelial cell monolayer permeability and that beta-adrenoceptor stimulation has the opposite effect. Reverse transport results obtained with beta-adrenoceptor stimulation seem controversial and deserve further study. These results also support in vivo findings that demonstrated adrenergic influences on blood brain barrier permeability.

Adrenergic Agents↗
PubMed1995

Low-efficiency (macro-)pinocytic internalization of non-pathogenic Escherichia coli into HEp-2 cells.

HEp-2 cells internalize non-pathogenic Escherichia coli bacteria by a low-efficiency internalization mechanism which is upregulated in Pho-derepressed strains (as shown by Sinai and Bavoil in 1993), and is independent of microfilament integrity but requires functional microtubules. Here, we further characterize the microtubule requirement of this pathway using various effectors of microtubule integrity and function. Furthermore, we show that internalization is enhanced upon treatment with monodansylcadaverine, a specific inhibitor of receptor mediated endocytosis, and is insensitive to brefeldin A, which promotes the microtubule-dependent reorganization of the endosome. An assay system is also described to directly evaluate the contribution of pinocytosis to this pathway based on the ability of the bacteria to cointernalize and consequently colocalize with the fluid-phase marker, Texas-red-conjugated dextran (TRD). Using this assay, Hoescht-stained bacteria were observed in TRD-containing vesicles in numbers that are consistent with their observed internalization rate. Overall, these data are strongly supportive of the existence of a low-efficiency macropinocytic mechanism of entry for these non-pathogenic bacteria. Moreover, the observed requirements for host tyrosine kinase and protein kinase C activities suggest that it is inducible.

Antifungal Agents↗
PubMed2005

Vascular damage by unstable hemoglobins: the role of heme-depleted globin.

The study compared the damage inflicted to endothelial cells (ECs) by intact hemoglobin (Hb) and isolated chains. To compare optional in vivo contact of acellular Hb with the endothelium, oxy-forms of Hb and its isolated alpha- and beta-chains existing in the thalassemias were added to primary confluent cultures of bovine aorta EC. Cell damage was followed by morphological changes or leakage of lactic dehydrogenase and pre-inserted 51Cr from the cells, followed for 27 h. Under these experimental conditions, Hb did not affect the cells but its chains inflicted damage, beta- more than alpha-chains. Based on the literature and our data, we hypothesized that hemin and/or globin should be responsible for the increased endothelial damage by beta-chains. While hemin hardly affected ECs, globin, unlike the plasma protein hemopexin, was harmful. Since hemin release leaves globin with a large hydrophobic surface, the globin-damage appears to result from adsorptive pinocytosis to endothelial membrane.

Animals↗